Docsity
Docsity

Prepare for your exams
Prepare for your exams

Study with the several resources on Docsity


Earn points to download
Earn points to download

Earn points by helping other students or get them with a premium plan


Guidelines and tips
Guidelines and tips

Environmental Factors Influencing Human Growth and Pubertal Development, Lecture notes of Nutrition

The complex relationship between hereditary and environmental factors that impact postnatal growth and pubertal development in humans. The paper discusses various factors, including intrauterine growth, urbanization, nutrition, disease, and socioeconomic status, that can influence growth and maturation. It also examines the impact of prenatal and postnatal factors on final height.

Typology: Lecture notes

2021/2022

Uploaded on 09/27/2022

attourney
attourney 🇬🇧

3.7

(10)

7 documents

1 / 6

Toggle sidebar

Related documents


Partial preview of the text

Download Environmental Factors Influencing Human Growth and Pubertal Development and more Lecture notes Nutrition in PDF only on Docsity! Environmental Health Perspectives Supplements 101 (SuppL 2): 39-44 (1993) Environmental Factors Influencing Growth and Pubertal Development by Henriette A. Delemarre-van de Waal Postnatal growth is based on hereditary signals and environmental factors in a complex regulatory network. Each factor must be in an optimal state for normal growth of the child. Fetal conditions may also have consequences on postnatal height. Intrauterine growth retardation can be recovered postnatally, although postnatal growth remains depressed in about one-third of cases. After birth, the environment may exert either a positive or negative effect on growth. In underdeveloped countries, malnutrition plays a major role in inhibiting the growth process. Children from families of higher socioeconomic classes are taller than their coevals in the lower socioeconomic groups. Urbanization also has a positive effect on growth. Better child care is supported by sufficient food supply, appropriate health and sanitation services, and a higher level of education. Over the last century, these factors have induced a taller stature and a more rapid maturity in Europe, North America, and Australia; a phenomenon which has been referred to as "the secular trend" in growth. Recently, a secular trend has also been reported in some developing countries. Although urbanization in general appears to be associated with better conditions of living, this is not the case in the slums of South America or in Africa where rural children are better off than children living in the poor cities. This paper describes in more detail the different hereditary and environmental factors that act duringthe fetal period and postnatally, and which play a role in human growth and pubertal development. Introduction Growth is the result of the concerted effect of a complex network of many regulatory factors with varying interac- tions. Each individual has a genetic base with a definite growth potential, which may be modulated by these fac- tors both in the prenatal period and in postnatal life (1). Optimal growth can only be achieved when all these factors operate in harmony. Postnatal growth is determined by hereditary factors, the length of the newborn baby which was achieved pre- natally, and environmental factors to which the child is exposed during the growth period postnatally (Fig. 1). During puberty, the pubertal growth spurt produces an extra increase in height, but thereafter growth soon ends (2). There is a close relationship between pubertal develop- ment and the growth process, and the onset of puberty is more correlated with skeletal age than with chronological age (3). Therefore, when growth is retarded, there will usually be an associated retardation of skeletal matura- tion, and this will result in delayed puberty as an additional complication. In many countries, the environmental condi- tions are such that there is incomplete expression of Department of Pediatrics, Free University Hospital, P. 0. Box 7057, 1007 MB Amsterdam, The Netherlands. This manuscript was presented at the Conference on the Impact of the Environment on Reproductive Health that was held 30 September4 October 1991 in Copenhagen, Denmark. hereditary components, and this may have consequences on prenatal and postnatal growth. Genetic Factors It is well known that the parents' height has an influence on the stature of their children. However, the relationship between the height of the baby and that of the parents is not appareilt at birth but becomes more evident toward the age of 2 years, and thereafter the correlation becomes greater with increasing age (4). The Louisville Twin Study examined height data longitudinally from birth to matu- rity in twin families, and from this it was estimated that heredity accounted for 90% or more of the factors that de- termined height from the age of 6 years and after (5). These investigators observed a substantial and constant correlation between the height of the children and their parents from the age of3 years and onwards. Monozygotic twins, with identical genetic composition, had a greater difference in final height when reared apart than when reared together. However, this difference was less than the difference between dizygotic twins (6). The difference in height ofmonozygotic twins is probably caused by environ- mental factors. Body proportions are probably also under the influence of genetic control. In relative terms, the Australian Abori- gines and the Africans in Ibadan have the longest legs (1). During the growth phase, the gain of leg length in com- parison to gain in total length can be proportionally H. A. DELEMARRE-VAN DE WAAL psychosocial genetics season/climate prenatal growth postnatal growth physical activity nutrition urbanization disease socioeconomics FIGURE 1. Factors influencing postnatal growth. different in different populations. As an example, Chinese children at a young age have relatively long legs, but as they become taller they gain less leg length per unit length of sitting height than London children. The mixing of races produces children with stature and body proportions intermediate between the parental populations (1). Hereditary diseases and chromosomal aberrations may affect the growth process, usually exerting a suppressive influence. Thrner's syndrome (karyotype 45,XO), other X chromosomal abnormalities, and Klinefelter's syndrome are well-known diseases associated with either short or long stature. In spite of many new developments in endo- crine therapy such as growth hormone treatment for Thrner's syndrome, it is difficult to manipulate genetically defined growth characteristics (7). Environmental Factors Prenatal Growth The fetus does not develop optimally in poor environ- mental conditions. Weight gain is the first parameter to be inhibited, but after prolonged inadequacy height is also negatively affected (8). Environmental conditions account for about 60% of the variability ofbirth weight and genetic factors for the remaining 40% (9). Such environmental factors, among others, include maternal age, order of birth, and crowding within the uterus (10). Primiparous mothers either older than 38 or younger than 20 years of age have an increased risk of giving birth to small-for-date babies (11). First-born babies have a birth weight of about 100 g less than second or third babies, and in multiple pregnancies the weight gain of each fetus after the 30th week of gestation is less than that of single-pregnancy fetuses (12). An inhibiting effect on fetal growth is also exerted by illness in the mother, malnutrition, therapeutic drug treatment, alcohol and other social drug addiction, and cigarette smoking. Offspring of mothers with insulin-dependent diabetes are known to be at greater risk of developing congenital malformations, and the incidence of abnormalities is rela- ted to poor control of blood sugar levels in the first trimes- ter. It is important to ensure precise diabetic control early in gestation so that a more normal environment of glucose, insulin, and ketone levels is maintained in order to dimin- ish congenital anomalies (13). Antihypertensive and anti- convulsant drugs in particular are therapeutic agents that have a disturbing effect on fetal growth and morpho- genesis (14). Alcohol, drug addiction, and smoking may have a severe effect on the height and weight of babies (15-17), and smoking is known to increase the risk of prematurity (18). The underlying mechanisms appear to be maternal mal- nutrition with a deficiency of trace elements and placental dysfunction in addition to a direct toxic effect on the fetus. Alcohol addiction also increases the incidence of congeni- tal malformations (19). Malnutrition is still a worldwide problem. Fetal growth is inhibited by maternal malnutrition whether it is a defi- ciency ofprotein, calories, or trace elements. Furthermore, malnutrition may reduce fetal brain development (20). There are three phases of cellular growth and organ development, the first being a phase of cell proliferation, followed by a phase of proliferation with concomitant hypertrophy, and a third phase of hypertrophy alone. Disturbances of the proliferation phase ofbrain tissue, for example, results in a lower DNA and protein content, which is irreversible and from which the brain does not recover. Therefore, the earlier the phase during which malnutrition occurs, the more serious is the lack of brain growth. This explains why fetal malnutrition may induce long-term damage to the child. Since brain development continues postpartum into infancy it is clear that postnatal malnutrition may also affect the brain (21). Climate also has a regulatory effect on birth weight. Babies born in the mountains of Peru on average weigh 1500 g less than the-newborns of Lima (22).- The socioeconomic environment in even the well-devel- oped countries is still undergoing changes, and modern women have the opportunity of working in male-oriented industries. Over the next decade, information will be gathered about possible factors such as toxins and work- load, which may interfere with providing a safe internal environment for the developing fetus (23). The prenatal effects on weight and height may disappear postnatally. Catch-up growth with respect to height occurs during infancy, but this may be incomplete (24), and the final height may be severely compromised by prenatal factors. Postnatal Growth Postnatal environmental factors affecting growth include nutrition, disease, socioeconomic status, urbanization, physi- cal activity, climate, and psychosocial deprivation. Nutrition. Malnutrition results in failure to grow, involving both weight and height. Increased growth hor- mone secretion occurs in protein malnutrition, presumably inducing mobilization of the remaining fat tissue (25). On the other hand, growth hormone levels are decreased in calorie malnutrition. When malnutrition is corrected, the affected children soon recover, and when this reversal occurs at a young age, most children will attain a complete remission in height and weight to equal their siblings before puberty (26,27). However, this is not always the case, probably because of long-term deficits, and the home diet following hospital admission may play a role in such an 40 ENVIRONMENT GROWTH, AND PUBERTY 43 prenatal as well as postnatal growth. Before the age of 2 years, there is no correlation between the height of the parents and the height of the offspring, but there is a direct correlation after the age of 2. Prenatal growth factors include maternal age, parity, alcohol consumption, drug addiction, smoking, therapeutic medication, climate, altitude, and malnutrition. Prenatal malnutrition has an effect on the developing brain, and the final effects produced depend on the age at which the malnutrition occurs. Postnatal growth is affected by nutrition, socioeconomic factors, disease, urbanization, psychosocial stress, and physical activity. There is a complex interaction among these different factors, and periods of retardation can be compensated by ensuing catch-up growth if the adverse factors are remedied. Final height is determined by an interaction of growth rate and age at puberty, however, optimal conditions that stimulate growth may also advance the age of puberty with a negligible net effect on adult height. REFERENCES 1. Eveleth, P. B., and Tanner, J. M. Worldwide Variation in Human Growth. Cambridge Univer-sity Press, Cambridge, 1990. 2. Bourguignon, J. P. Linear growth as a function of age at onset of puberty and sex steroid dosage, therapeutic implications. Endocrinol. Rev. 9: 467-488 (1988). 3. Marshall, W. A., and de Limongy, Y. Skeletal maturity and prediction of age at menarche. Ann. Hum. Biol. 3: 235-245 (1976). 4. Smith, D. W., Truog, W., and Rogers, J. E. Shifting linear growth during infancy: illustration of genetic factors in growth from fetal life through infancy. J. Pediatr. 89: 225-230 (1976). 5. Philips, K., and Matheny, A. P. Quantitative genetic analysis of longitudinal trends in height: preliminary results from the Louisville Twin Study. Acta Genet. Med. Gemellol. 39: 143-163 (1990). 6. Shields, J. Monozygotic T\wins. Oxford University Press, London, 1962. 7. Ranke, M. B., and Rosenfeld, R. Thrner's Syndrome and Growth Promoting Therapies. Excerpta Medica, Amsterdam, 1991. 8. Usher, R. H., and McLean, F. H. Normal fetal growth and the significance of fetal growth retardation. In: Scientific Foundations of Paediatrics (J. A. Davis, J. Dobbing, and W. Heinemunn, Eds.), Medical Books Ltd., London, 1974, pp. 69-79. 9. Polani, P. E. Size of Birth. Ciba Foundation Symposium, Exerpta Medica, Amsterdam, 1974. 10. Giovannelli, G., Bernasconi, S., and Ghizzoni, L. Environmentai fac- tors and growth. In: Growth Abnormalities (J. R. Bierich, E. Cac- ciarci, and S. Raiti, Eds.), (Serono Symposia Publications, Vol. 56) Raven Press, New York, 1989. 11. Lobl, M., Welcher, D. W., and Mellits, E. D. Maternal age and intellectual functioning of offspring. Johns Hopkins Med. J. 128: 347- 361 (1971). 12. Underwood, L. E. In: Textbook of Endocrinology (J. P. Wilson and D. W. Foster, Eds.), Saunders Co., Philadelphia, 1985. 13. Miodovnik, M., Mimouni, F, Dignan, P. S. J., Berk, M. A., Ballard, J. L., Siddiqi, T. A., Khoury, J., and Tsang, R. C. Major malformations in infants of IDDM women. Diabetes Care 11: 713-718 (1988). 14. Hill, R. M., and Tennyson, L. M. Maternal drug therapy: effect on fetal and neonatal growth and neurobehavior. Neurotoxicology 7: 121-140 (1986). 15. Jones, K. L., Smith, D. W., Ulleland, C. N., and Streissguth, A. P. Pattern of malformation of chronic alcoholic mothers. Lancet i: 1267- 1268 (1973). 16. Fulroth, R. Philips, B., and Durand, D. J. Perinatal outcome of infants exposed to cocaine and/or heroin in utero. Am. J. Dis. Child. 143: 905- 910 (1989). 17. Hoff, C., Wertelecki, W., Blackburn, W. R, Mendenhall, H., Wiseman, H., and Stumpe, A. Trend associations of smoking with maternal, fetal and neonatal morbidity. Obstet. Gynecol. 68: 317-321 (1986). 18. Fedrick, J., and Adelstein, P. Factors associated with low birth weight of infants delivered at term. Br. J. Obstet. Gynecol. 85: 1-7 (1978). 19. Streissguth, A. P, Heiman, C. S, and Smith, D. W. Intelligence, behaviour and dysmorphogenesis in the fetal alcohol syndrome: a report on 20 patients. J. Pediatr. 92: 363-367 (1978). 20. Winick, M. Cellular growth during early malnutrition. Pediatrics 47: 969-978 (1971). 21. Winick, M., and Rosso, P. The effect of severe early malnutrition on cellular growth of human brain. Pediatr. Res. 3: 181-184 (1969). 22. Krugher, H, and Arias-Stella, J. The placenta and the newborn infant at high altitudes. Am. J. Obstet. Gynecol. 106: 586-591 (1970). 23. McCloy, E. C. Work, environment and the fetus. Midwifery 5: 53-62 (1989). 24. Fitzhardinge, P. M., Inwood, S. Long-term growth in small-for-date children. Acta Paediatr. Scand. (suppl.) 349: 27-33 (1989). 25. Primestone, B. L, Barbezat, G, Hansen, J. D. L., and Muriay, P. Studies on growth hormone secretion in protein-calorie malnutrition. Am. J. Clin. Nutr. 21: 482 (1968). 26. Garrow, J. S., and Pike, M. C. The long-term prognosis of severe infantile malnutrition. Lancet i: 1-4 (1967). 27. Hansen, J. D. L., Freesemann, C, Moodie, A. D, and Evans, D. E. What does nutritional growth retardation imply? Pediatrics 47: 299- 313 (1971). 28. MacWilliam, K. M., and Dean, R. F. A. The growth of malnourished children after hospital treatment. East African Med. J. 42: 297-304 (1965). 29. Graham, G. G. The later growth of malnourished infants: effects of age, severity and subsequent diet. In: Calorie Deficiencies and Pro- tein Deficiencies (R. A. McCance and E. M. Widdowson, Ed.), Church- ill, London, 1968, pp. 301-316. 30. Brown, G. M., Seggie, J. A., Chambers, J. W., and Ettigi, P. G. Psycho- neuro-endocrinology and growth hormone: a review. Psychoneuroen- docrinology 3: 131-153 (1978). 31. Eisenberg, E. Toward an understanding of reproduction function in anorexia nervosa. Fertil. Steril. 36: 543-550 (1981). 32. Blanco, R. A., Acheson, R. M., Canosa, C., and Salomon, J. B. Height, weight and lines of arrested growth in young Guatemalan children. Am. J. Physical. Anthropol. 40: 39-48 (1974). 33. Groll, A., Candy, D., Preece, M., Tanner, J., and Harries, J. Short stature as the primary manifestation of coeliac disease. Lancet ii: 1097-1099 (1980). 34. Prader, A., Tanner, J. M, and von Harnack, G. A. Catch-up growth following illness or starvation. J. Pediatrics 62: 646-659 (1963). 35. Tanner, J. M. Catch-up growth in man. Br. Med. Bull. 37: 233-238 (1981). 36. Goldstein, H. Factors influencing the height of seven-year-old chil- dren. Results from the National Child Development Study. Hum. Biol. 43: 92-111 (1971). 37. Douglas, J. W. B., and Simpson, H. R. Height in relation to puberty, family size and social class. Millbank Mem. Fund Q. 42: 20-35 (1964). 38. Brindtland, G., Liestol, K., and Walloe, L. W. Height, weight and men- archeal age of Oslo school children during the last 60 years. Ann. Hum. Biol. 7: 307-322 (1980), 39. Cook, J., Altman, D. G, Morre, D. M. C., TopA S. G., Holland, W. W., and Elliot, A. A survey of the nutritional status of schoolchildren. Re- lation between nutrient intake and socio-economic factors. Br. J. Prevent. Soc. Med. 27: 91-99 (1973). 40. Tanner, J. M., and Eveleth, P. B. Urbanisation and growth. In: Man in Urban Environments (G. A. Harrison and J. B. Gibson, Eds.), Claren- don Press, Oxford, 1976, pp. 144-166. 41. Hamill, P. V. V., Johnston, F. E., and Lereshow, S. Height and Weight of Children: Socio-Economic Status. Department of Health, Educa- tion and Welfare Publication, No. 73-1606, Vital Health Statistics Series 11, No. 119. U.S. Goverment Printing Office, Washington, DC, 1972. 42. Jones, D. L., Hemphill, W., and Meyers E. S. A. Height, weight and other physical characteristics of New South Wales children. Part 1. Children aged five years and over. New South Wales Department of Health, G.96543-a K5705, Sydney, Australia, 1973. 43. Villarejos, V. M., Osborne, J. A., Payne, F. J., and Arguedes, J. A. Heights and weights of children in urban and rural Costa Rica. 44 H. A. DELEMARRE-VAN DE WAAL Environ. Child Health 17: 31-43 (1971). 44. Paigen, B., Goldman, L. R., Magnant, M. M., Highland, J. H., and Steegmann, A. T. Growth of children living near the hazardous waste site, Love Canal. Hum. Biol. 59: 489-508 (1987). 45. Kriger, I., and Mellinger, R. C. Pituitary function in the deprivation syndrome. J. Pediatr. 79: 216-225 (1971). 46. Friend, G. E., and Bransby, E. R. Physique and growth of schoolboys. Lancet ii: 677-681 (1947). 47. Marshall, W. A. Evaluation of growth rate in height over periods of less than one year. Arch. Dis. Child. 46 :414-420 (1971). 48. Leonard, W. R. Nutritional determinants of high altitude growth in Nunoa, Peru. Am. J. Physical. Anthropol. 80: 341-352 (1989). 49. Thomson, A. M. Maternal stature and reproductive efficiency. Eugenics Rev. 51: 157-162 (1954). 50. Frisancho, A. R., Sanchez, J., Pollardel, D., and Yanez, L. Adaptive significance of small body size under pooIr socioeconomic conditions in Southern Peru. Am. J. Physical Anthropol. 39: 255-262 (1973). 51. Fischbein, S. Intra-pair similarity in physical growth in monozygotic and of dizygotic twins during puberty. Ann. Hum. Biol. 3: 205-210 (1977). 52. Roede, M. J., and Wieringen, J. C. Gro'wth diagrams 1980. T. Soc. Gezondheidszorg 63 (suppl.): 1-34 (1985). 53. Danker-Hopfe, H. Die Sakulare Veranderung des Menarchealters in Europa. Schweizerbart, Stuttgart, 1984. 54. Eveleth, P. B. Eruption of permanent dentition and menarche of Ameiican children living in the tropics. Human Biol. 38: 60-70 (1966). 55. Liestol, K. Social conditions and menarcheal age: the importance of early years of life. Ann. Hum. Biol. 9: 521-538 (1982). 56. Stanhope, R., and Brook, C. G. D. In: Clinical Paediatric Endocrinol- ogy: Disorders of Puberty (C. G. D. Brook, Ed.), Blackwell, Oxford, 1989, pp. 189-212. 57. Pasquino, A. M., Cives, C., Maciocci, M., Tebaldi, L., Musleh, M., and Boscherini, B. Transient true precocious puberty. A report of five cases. Eur. J. Pediatr. 148: 735-736 (1989). 58. Fontoura, M., Brauner, R., Prevot, C., and Rappaport, R. Precocious puberty in girls: early diagnosis of a slowly progressing variant. Arch. Dis. Child. 64: 1170-1176 (1989). 59. Kaplan, S. L., and Grumbach M. M. Pathogenesis of sexual precocity. In: Control of the Onset of Puberty, II (M. M. Grumbach, P. C. Sizonanko, and M. L. Aubert, Eds.), Williams and Wilkins, Baltimore, MD, 1990, pp. 620-664. 60. Boneh, A., Landau, H., and Friedlandei- N. Age and seasonal factors in the incidence of premature sexual development in girls in the Jerusalem area. Clin. Invest. Med. 12: 172-174 (1989). 61. Fara, G. M., Del Corvo, G., Bernuzzi, S., Bigatello, A., Di Pietro, C., Scaglioni, S., and Chiumello, G. Epidemic of breast enlargement in an Italian school. Lancet ii: 295-297 (1979). 62. Bongiovanni, S. M. An epidemic of premature thelarche in Puerto Rico. J. Pediatr. 103: 245-246 (1983). 63. Proos, L. A., Holvander, Y., and Tuvvemo, T. Height and weight at menarche for Indian girls adopted to Sweden (abstract no. 4). In: Third International Conference on the Control of the Onset of Puberty, Amsterdam, 1989. 64. Oostdijk, W., Yap, Y. N., Doude van TroostwAijk, M. L., Gevers, E. F., Brand, R., Verhulst, F. C., and Drop, S. L. S. Final height and timing of puberty of adopted children in the Netherlands. Hormone Res. 35(2): 24 (1991).
Docsity logo



Copyright © 2024 Ladybird Srl - Via Leonardo da Vinci 16, 10126, Torino, Italy - VAT 10816460017 - All rights reserved